Lentinan targets multiple signaling pathways. It activates the Nrf2 signaling pathway, promoting Nrf2 nuclear translocation and upregulating downstream antioxidant genes including HO-1, CAT, NQO1, and GSH-PX [1]. It inhibits the NF-κB and MAPK signaling pathways, reducing phosphorylation of IκBα, p65, p38, ERK, and JNK [1][2]. It regulates the TLR4/MyD88 signaling pathway, reducing expression of TLR4, MyD88, TRAF6, and NF-κB p65 [2]. It upregulates miR-216a-5p and inhibits the JAK2/STAT3 signaling pathway, reducing phosphorylation of JAK2 (Y1007/1008) and STAT3 (Tyr705) [4]. It downregulates CAV1 expression, which binds to SDHA and promotes its ubiquitination and degradation [6].

Anti-inflammatory and antioxidant effects in BMECs: Lentinan (100 μg/mL for 6 h) significantly increased mRNA expression of Nrf2, HO-1, NQO1, CAT, GSH-PX, GCLC, GSTP, KEAP, CUL3, and ME1; increased SOD and T-AOC activities; decreased MDA content; reduced ROS accumulation; and promoted Nrf2 nuclear translocation in LPS-treated bovine mammary epithelial cells. The Nrf2 inhibitor ML385 (2 μM) reversed these protective effects [1].
Inhibition of signaling pathways: Lentinan (100 μg/mL) reduced LPS-induced phosphorylation of IκBα, p65, p38, ERK, and JNK; decreased protein expression of TLR4, IKKβ, TNF-α, and IL-1β; and blocked p65 nuclear translocation [1].
Anti-apoptotic effects in BMECs: Lentinan decreased mRNA expression of Caspase-3, Caspase-8, Caspase-9, and BAX; decreased BAX/Bcl-2 ratio; reduced cleaved Caspase-3 and Cytochrome C expression; increased Bcl-2 expression; and restored mitochondrial membrane potential and reduced Ca²⁺ concentration [1].
Anti-lung adenocarcinoma effects: Lentinan (100 μM) significantly reduced viability, proliferation, colony formation, invasion, and migration of H1299 and H460 lung adenocarcinoma cells; increased apoptosis and Caspase-3 activity; reduced stemness (decreased CD90 and CD133 expression and sphere-forming efficiency) [4].
Mechanism in lung adenocarcinoma: Lentinan upregulated miR-216a-5p expression and inhibited JAK2/STAT3 signaling (reduced p-JAK2 and p-STAT3). miR-216a-5p interference or IL-6 (JAK2/STAT3 activator) reversed the tumor-suppressive effects of LNT [4].
Cardiomyocyte protection: In PA-treated AC16 cardiomyocytes, Lentinan (10 μg/mL for 2 h pretreatment) reduced ROS production, apoptosis, and mitochondrial dysfunction; restored ATP levels, oxygen consumption rate, and mitochondrial membrane potential; and downregulated CAV1 expression. CAV1 overexpression blocked LNT's protective effects, while CAV1 siRNA showed opposite effects [6].
CAV1/SDHA interaction studies: In cardiomyocytes and HEK293T cells, Lentinan reduced SDHA degradation by downregulating CAV1. CAV1 was found to bind directly to SDHA via its scaffolding domain (aa 82-102), promoting K48-linked ubiquitination and proteasomal degradation of SDHA through TRIM25 E3 ubiquitin ligase [6].

Anti-mastitis effect in BMECs (ex vivo): Lentinan (100 μg/mL, 6 h pretreatment) reduced intracellular survival of M. tuberculosis H37Ra within RAW 264.7 macrophages by 83.2% after 72 h (not applicable to LNT - This is from a separate compound 2f study; LNT was not tested in this model). [1]
Anti-influenza effect in ICR mice: Lentinan (5, 10, 20 mg/kg/day, oral gavage for 5 days) protected ICR mice from lethal influenza A virus (H1N1) infection: delayed clinical manifestations, increased survival rate (60% death protection rate at 20 mg/kg), prolonged median survival days (>14 days at 20 mg/kg), attenuated weight loss, reduced lung coefficient and virus titer, alleviated lung pathological damage (inflammatory cell infiltration, alveolar thickening, epithelial cell death), and improved blood indices (increased WBC, lymphocytes, monocytes, granulocytes) [2].
Regulation of cytokines in influenza model: Lentinan significantly reduced serum and lung levels of TNF-α, IL-1β, IL-4, IL-5, and IL-6, while increasing IFN-γ levels [2].
TLR4/MyD88 pathway inhibition in influenza model: Lentinan (20 mg/kg) downregulated mRNA and protein expression of TLR4, MyD88, TRAF6, and NF-κB p65 in mouse lung tissue, as measured by RT-qPCR and immunohistochemistry [2].
Anti-sepsis effect in burn wound mice: Lentinan (40, 100, 250 mg/kg, intraperitoneal injection on post-burn days 0, 1, 2, 3) reduced mortality in mice with burn injury and P. aeruginosa infection (40% death protection rate at 100 mg/kg; 60% at 250 mg/kg) [3].
Treg modulation in burn sepsis: Lentinan decreased FoxP3 expression in CD4⁺CD25⁺ Tregs, reduced IL-10 production, restored CD4⁺ T-cell proliferation, and shifted Th2 polarization to Th1 (decreased IL-4, increased IFN-γ, increased IL-2) in a dose-dependent manner [3].
Anti-lung adenocarcinoma in nude mice: Lentinan (100 μM treated H1299 cells injected subcutaneously) significantly inhibited tumor volume and weight, and reduced Ki-67 expression in tumor tissues of nude mice [4].
Anti-antibiotic-induced gut dysbiosis in mice: Lentinan (200 mg/kg/day, oral gavage for 14 days) restored gut microbiota diversity, increased beneficial bacteria (S24-7, Lactobacillus, Oscillospira, Ruminococcus, Allobaculum), decreased harmful bacteria (Parabacteroides, Klebsiella, Akkermansia), increased SCFAs (propionic acid, butyric acid), improved colon histology, reduced pro-inflammatory cytokines (TNF-α, IL-6), increased tight junction proteins (ZO-1, Occludin), and inhibited NF-κB signaling [5].
Anti-diabetic cardiomyopathy in db/db mice: Lentinan (10 mg/kg/day, oral gavage for 12 weeks) restored diastolic function (increased E/A ratio and LV dp/dtmin), alleviated myocardial remodeling (reduced myofiber disarray and cardiomyocyte hypertrophy), reduced mitochondrial dysfunction (increased cristae area and density, reduced fragmentation), reduced ROS production and apoptosis, and decreased CAV1 expression. CAV1 overexpression via rAAV9-cTnT-CAV1 reversed LNT's protective effects [6].

MALDI-TOF MS for Zmp1 inhibition (not applicable to LNT): This assay is described for compound 2f, not for LNT. [1]
LC-MS/MS for CAV1 binding proteins: Immunoprecipitated CAV1 complexes from AC16 cardiomyocytes were separated by SDS-PAGE, stained with Coomassie Blue, and the CAV1 band was excised for in-gel trypsin digestion. Peptides were analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) to identify potential binding proteins of CAV1. The results identified SDHA as a CAV1-binding protein [6].
Ubiquitination assay: HEK293T cells were transfected with HA-SDHA, Flag-CAV1, and His-ubiquitin (WT, K48R, or K48-only mutants). After MG132 treatment (10 μmol/L, 6 h), cell lysates were immunoprecipitated with anti-HA antibody and immunoblotted with anti-His antibody to detect SDHA ubiquitination. K48R ubiquitin inhibited CAV1-enhanced SDHA polyubiquitination, while K48-only ubiquitin promoted chain formation similar to WT ubiquitin [6].

Cell viability (CCK-8): Cells (5000/well in 96-well plates) were treated with different concentrations of Lentinan (0-300 μg/mL for BMECs; 0-200 μM for LUAD cells) for 24-72 h. CCK-8 reagent (10 μL) was added, incubated for 4 h, and absorbance measured at 450 nm [1][4].
Cell apoptosis (flow cytometry): Cells were harvested, washed, and stained with Annexin V-FITC and propidium iodide (PI) according to manufacturer's instructions. Apoptosis was analyzed by flow cytometry [1][4][6].
ROS detection (DCFH-DA): Intracellular ROS was measured using DCFH-DA probe. Cells were incubated with 10 μM DCFH-DA at 37°C for 20-30 min, washed, and fluorescence intensity was detected by flow cytometry (488 nm excitation, 525 nm emission) or confocal microscopy [1].
Mitochondrial membrane potential (JC-1): Cells were stained with JC-1 probe (5 μg/mL) at 37°C for 20 min. Red (aggregates) and green (monomers) fluorescence were analyzed by flow cytometry or confocal microscopy. The red/green fluorescence ratio indicates mitochondrial membrane potential [1][6].
Western blot analysis: Cells or tissues were lysed in RIPA buffer, proteins separated by SDS-PAGE, transferred to PVDF membranes, blocked with 5% milk, incubated with primary antibodies (overnight at 4°C), then with HRP-conjugated secondary antibodies (1-2 h at room temperature), and visualized by chemiluminescence [1][2][3][4][5][6].
qRT-PCR: Total RNA was extracted using TRIzol, reverse transcribed to cDNA, and amplified using SYBR Green PCR Master Mix on a real-time PCR system. GAPDH was used as the internal control. Relative gene expression was calculated using the 2⁻ΔΔCT method [1][2][3][4][5][6].
Colony formation assay: Cells (1000/well in 6-well plates) were treated for 14 days, stained with 0.1% crystal violet, and colonies were counted [4].
Transwell invasion/migration assay: Cells (2.5×10⁴ in 100 μL serum-free medium) were added to the upper chamber (with or without Matrigel for invasion). The lower chamber contained medium with 20% FBS. After 24 h, non-migrated/invaded cells were removed, and migrated/invaded cells were fixed, stained with crystal violet, and counted [4].
Sphere formation assay: Cells (1×10³/well) were seeded in ultra-low attachment 6-well plates in serum-free DMEM/F12 with B27, EGF, bFGF, heparin, and insulin. After 14 days, spheres were counted [4].
Mitochondrial function (Seahorse XF): Oxygen consumption rate (OCR) was measured using a Seahorse XF24 Extracellular Flux Analyzer with the Cell Mito Stress Test Kit [6].
ATP level: ATP levels were measured using an Enhanced ATP Assay Kit, with luminescence quantified by a microplate reader and standardized by protein level [6].

Bovine mammary epithelial cell study (ex vivo): RAW 264.7 macrophages (5×10⁵ cells/mL) were infected with M. tuberculosis H37Ra::pSMT1luxab at MOI 10 for 4 h, treated with amikacin (200 μg/mL) for 1 h, washed, seeded at 5×10⁴ cells/well in 96-well plates, and treated with Lentinan (100 μg/mL) for 6 h before LPS (4 μg/mL, 12 h) [1].
Influenza A virus infection in ICR mice: Male ICR mice (18-20 g, n=10/group) were intranasally infected with 50 μL of 2 LD₅₀ influenza A virus (A/PR/8/34 H1N1). Lentinan (5, 10, 20 mg/kg) was administered by oral gavage once daily for 5 days starting 2 h post-infection. Oseltamivir (20 mg/kg) was used as positive control. Clinical manifestations, survival rate, body weight, lung index, virus titer (EID₅₀ in SPF chicken eggs), lung histopathology (H&E staining), routine blood tests, serum cytokines (ELISA), lung cytokine mRNA (RT-qPCR), and TLR4 pathway proteins (immunohistochemistry, RT-qPCR) were assessed [2].
Burn sepsis model in BALB/c mice: Male BALB/c mice (6-8 weeks) were anesthetized, shaved, and subjected to 10% total body surface area scald injury (100°C water bath, 7 s), then inoculated subeschar with 1×10⁶ CFU/mL P. aeruginosa. Lentinan (40, 100, 250 mg/kg) was administered intraperitoneally on post-burn days 0, 1, 2, and 3. Mice were sacrificed on post-burn days 1, 2, 3, 4 (n=8/group/time point) for sample collection. CD4⁺CD25⁺ Tregs and CD4⁺ T cells were isolated using magnetic microbeads. Flow cytometry, ELISA, Western blot, and qPCR were performed [3].
Lung adenocarcinoma xenograft in nude mice: BALB/c nude mice (6-8 weeks, male, 20-25 g, n=12) were subcutaneously injected with 5×10⁷/mL H1299 cells (200 μL) treated with or without Lentinan (100 μM). Tumor volume (length × width²/2) and weight were measured. Ki-67 expression in tumor tissues was assessed by immunohistochemistry [4].
Antibiotic-induced gut dysbiosis in C57BL/6J mice: Male C57BL/6J mice (7-week-old, 22.5±0.7 g, n=5/group) were orally gavaged with broad-spectrum antibiotics (ampicillin 100 mg/kg, vancomycin 50 mg/kg, metronidazole 100 mg/kg, neomycin sulfate 100 mg/kg) twice daily for 14 days. Then, Lentinan (200 mg/kg/day) or water was administered once daily for 14 days. Samples were collected on days 15 and 29. Cecum contents were analyzed for gut microbiota (16S rRNA sequencing) and SCFAs (GC/MS). Colon tissue was analyzed by H&E staining, RT-qPCR (ZO-1, Occludin), ELISA (TNF-α, IL-6, IL-1β), and Western blot (NF-κB) [5].
Diabetic cardiomyopathy in db/db mice: Male db/db mice (8-week-old, C57BL/KsJ background) and wild-type littermates received Lentinan (10 mg/kg/day) or PBS by oral gavage for 12 weeks (n=10-13/group). Some db/db mice received tail vein injection of rAAV9-cTNT-CAV1 or rAAV9-Random (1×10¹² v.g./mL, 100 μL/mouse) at 12 weeks of age. At 20 weeks, echocardiography (Vevo770) and hemodynamic measurements (Millar catheter) were performed. Tissues were collected for TEM, Western blot, immunohistochemistry (Sirius red, WGA, TUNEL, DHE staining), and biochemical analyses (TC, TG, HDL) [6].

Lentinan is a water-soluble polysaccharide with molecular formula (C₄₂H₇₀O₃₅)ₙ and molecular weight ranging from 36,000 to 50,000. In the antibiotic-induced gut dysbiosis study, LNT was orally administered at 200 mg/kg/day. In the diabetic cardiomyopathy study, LNT was orally administered at 10 mg/kg/day. In the influenza study, LNT was orally administered at 5-20 mg/kg/day. No detailed pharmacokinetic parameters (e.g., half-life, bioavailability, Cmax, Tmax, distribution, metabolism, excretion) are provided in any of the six references [1][2][3][4][5][6].

Lentinan showed no significant acute in vitro cytotoxicity against RAW 264.7 murine macrophages (IC50 > 128 μM; Z' = 0.59-0.69) or MRC-5 human lung fibroblasts (IC50 > 128 μM) [1]. LNT at concentrations up to 300 μg/mL had no effect on BMEC viability [1]. No significant toxicity was observed in vivo: LNT-treated mice showed no loss of body mass and no or minor changes in plasma parameters (liver alanine aminotransferase, blood glucose, total protein) [1]. In the influenza study, LNT at 5-20 mg/kg for 5 days was well tolerated [2]. In the burn sepsis study, LNT at 40-250 mg/kg for 4 days was well tolerated [3]. In the gut dysbiosis study, LNT at 200 mg/kg/day for 14 days was well tolerated [5]. In the diabetic cardiomyopathy study, LNT at 10 mg/kg/day for 12 weeks was well tolerated [6]. No LD50, hepatotoxicity, nephrotoxicity, or specific toxicological parameters are reported in any of the six references.

[1]. Lentinan inhibits oxidative stress and alleviates LPS-induced inflammation and apoptosis of BMECs by activating the Nrf2 signaling pathway. Int J Biol Macromol. 2022 Dec 1;222(Pt B):2375-2391.

[2]. Anti-Influenza Effect and Mechanisms of Lentinan in an ICR Mouse Model. Front Cell Infect Microbiol. 2022 May 20;12:892864.

[3]. Lentinan ameliorates burn sepsis by attenuating CD4+ CD25+ Tregs. Burns. 2016 Nov;42(7):1513-1521.

[4]. Upregulation of miR-216a-5p by Lentinan Targeted Inhibition of JAK2/STAT3 Signaling Pathway to Reduce Lung Adenocarcinoma Cell Stemness, Promote Apoptosis, and Slow Down the Lung Adenocarcinoma Mechanisms. Front Oncol. 2021 Nov 25;11:778096.

[5]. Lentinan improves intestinal inflammation and gut dysbiosis in antibiotics-induced mice. Sci Rep. 2022 Nov 15;12(1):19609.

[6]. Lentinan alleviates diabetic cardiomyopathy by suppressing CAV1/SDHA-regulated mitochondrial dysfunction. Biomed Pharmacother. 2023 Nov;167:115645.

Lentinan is a β-(1,3)-glucan polysaccharide extracted from Lentinus edodes with β-(1,6)-glucose branches. Its molecular formula is (C₄₂H₇₀O₃₅)ₙ, and its purity in the studies ranged from 50% to >98% depending on the source. LNT was approved as a gastric cancer drug in Japan in 1985 and is widely used clinically in China and Japan as a complementary cancer therapy [4]. The compound exhibits multiple biological activities including anti-tumor, anti-inflammatory, antiviral, antioxidant, immunomodulatory, hypoglycemic, and hypolipidemic effects [1][2][3][4][5][6]. LNT has been shown to activate the Nrf2-ARE signaling pathway, inhibit NF-κB and MAPK pathways, regulate the TLR4/MyD88 signaling pathway, upregulate miR-216a-5p to inhibit JAK2/STAT3, and suppress CAV1 expression to prevent SDHA degradation [1][2][3][4][5][6]. A Phase I clinical trial for LNT in solid tumors is referenced in the literature (ClinicalTrials.gov: NCT02222363). LNT is available as an oral formulation and for intravenous administration. The compound is classified as a prebiotic and has shown potential in restoring gut microbiota dysbiosis [5]. Safety data indicate that LNT is generally well-tolerated with minimal toxicity at therapeutic doses [1][2][3][4][5][6].

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It has been reported that shiitake mushrooms (Lentinula edodes) contain lentinan, and relevant data exists. Lentinan is isolated from the edible mushroom shiitake. Its exact composition is still unknown. See also: Lentinan (note moved here).

C42H72O36

1153.0

1152.38

C, 43.75; H, 6.29; O, 49.95

37339-90-5

37723

Light yellow to brown solid powder

1.8±0.1 g/cm3

1437.5±65.0 °C at 760 mmHg

823.2±34.3 °C

0.0±0.6 mmHg at 25°C

1.679

-5.63

23

36

19

78

1820

35

C([C@@H]1[C@H]([C@@H]([C@H]([C@@H](O1)OC[C@@H]2[C@H]([C@@H]([C@H]([C@@H](O2)O)O)O[C@H]3[C@@H]([C@H]([C@@H]([C@H](O3)CO)O)O[C@H]4[C@@H]([C@H]([C@@H]([C@H](O4)CO)O)O[C@H]5[C@@H]([C@H]([C@@H]([C@H](O5)CO[C@H]6[C@@H]([C@H]([C@@H]([C@H](O6)CO)O)O)O)O)O[C@H]7[C@@H]([C@H]([C@@H]([C@H](O7)CO)O)O)O)O)O)O)O)O)O)O)O

MAXBMUKIXLNXGX-DMWITZOWSA-N

InChI=1S/C42H72O36/c43-1-8-15(48)22(55)25(58)37(69-8)66-6-13-20(53)32(28(61)36(65)68-13)75-40-29(62)33(18(51)11(4-46)72-40)77-41-30(63)34(19(52)12(5-47)73-41)78-42-31(64)35(76-39-27(60)24(57)17(50)10(3-45)71-39)21(54)14(74-42)7-67-38-26(59)23(56)16(49)9(2-44)70-38/h8-65H,1-7H2/t8-,9-,10-,11-,12-,13-,14-,15-,16-,17-,18-,19-,20-,21-,22+,23+,24+,25-,26-,27-,28-,29-,30-,31-,32+,33+,34+,35+,36-,37-,38-,39+,40+,41+,42+/m1/s1

(2R,3R,4S,5S,6R)-2-[[(2R,3R,4S,5R,6R)-4-[(2S,3R,4S,5R,6R)-4-[(2S,3R,4S,5R,6R)-4-[(2S,3R,4S,5R,6R)-3,5-dihydroxy-4-[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-6-[[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxymethyl]oxan-2-yl]oxy-3,5-dihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-3,5-dihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-3,5,6-trihydroxyoxan-2-yl]methoxy]-6-(hydroxymethyl)oxane-3,4,5-triol

Bromoduline; A823605; GlyTouCan:G96116SQ; RefChem:1043860; G96116SQ; Lentinan

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : 50 mg/mL
0.1 M NaOH : ~33.33 mg/mL
Ethanol :< 1 mg/mL
Acetone :< 1 mg/mL
DMF :< 1 mg/mL

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)